Head‐to‐head comparison of sirolimus‐eluting stent versus bare metal stent evaluation of the coronary endothelial dysfunction in the same patient presenting with multiple coronary artery lesions: The CREDENTIAL study

Mischie, Alexandru; Nazzaro, Marco Stefano; Fiorilli, Rosario; Felice, Francesco De; Musto, Carmine; Confessore, Pierpaolo; Parma, Antonio; Boschetti, Carla; Violini, Roberto

doi:10.1002/ccd.24844

Cited by 10 publications

(6 citation statements)

References 18 publications

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“…By treating stenosis the ischemic trigger of angiogenesis is reduced [25] and this might be explained by the increase of VEGF levels [26]. This issue is relevant considering endothelial dysfunction after drug eluting stent apposition when compared with bare metal stent [27, 28]. …”

Section: Discussionmentioning

confidence: 99%

Prognostic Value of VEGF in Patients Submitted to Percutaneous Coronary Intervention

et al. 2014

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We examined the longitudinal changes of VEGF levels after percutaneous coronary intervention for predicting major adverse cardiac events (MACE) in coronary artery disease (CAD) patients. VEGF was measured in 94 CAD patients' serum before revascularization, 1-month and 1-year after. Independently of clinical presentation, patients had lower VEGF concentration than a cohort of healthy subjects (median, IQ: 15.9, 9.0–264 pg/mL versus 419, 212–758 pg/mL; P < 0.001) at baseline. VEGF increased to 1-month (median, IQ: 276, 167–498 pg/mL; P < 0.001) and remained steady to 1-year (median, IQ: 320, 173–497 pg/mL; P < 0.001) approaching control levels. Drug eluting stent apposition and previous medication intake produced a less steep VEGF evolution after intervention (P < 0.05). Baseline VEGF concentration <40.8 pg/mL conveyed increased risk for MACE in a 5-year follow-up. Results reflect a positive role of VEGF in recovery and support its importance in CAD prognosis.

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Section: Discussionmentioning

confidence: 99%

Prognostic Value of VEGF in Patients Submitted to Percutaneous Coronary Intervention

et al. 2014

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“…(3) Vasoconstriction at juxta-SES-implanted coronary segments, which results in the formation of AS in non-target vessels. In evaluating the endothelial function influenced by SES or bare metal stents, vasoconstriction induced by acetylcholine provocation test, as a hallmark of endothelial dysfunction, is elevated at juxta-SES-implanted coronary segments compared with that in the juxta-bare metal stents coronary segment in patients with multiple lesions (Mischie et al, 2013). This finding implies that RAPA may trigger the AS cascade, as impaired endothelial cell function initiates the formation of AS adjacent to the stented vascular segments (Bonetti et al, 2003), with more in-stent restenosis at the edge of SES.…”

Section: The Main Challenge To the Application Of Rapamycinmentioning

confidence: 99%

Rapamycin: A Bacteria-Derived Immunosuppressant That Has Anti-atherosclerotic Effects and Its Clinical Application

et al. 2019

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Atherosclerosis (AS) is the leading cause of stroke and death worldwide. Although many lipid-lowering or antiplatelet medicines have been used to prevent the devastating outcomes caused by AS, the serious side effects of these medicines cannot be ignored. Moreover, these medicines are aimed at preventing end-point events rather than addressing the formation and progression of the lesion. Rapamycin (sirolimus), a fermentation product derived from soil samples, has immunosuppressive and anti-proliferation effects. It is an inhibitor of mammalian targets of rapamycin, thereby stimulating autophagy pathways. Several lines of evidence have demonstrated that rapamycin possess multiple protective effects against AS through various molecular mechanisms. Moreover, it has been used successfully as an anti-proliferation agent to prevent in-stent restenosis or vascular graft stenosis in patients with coronary artery disease. A thorough understanding of the biomedical regulatory mechanism of rapamycin in AS might reveal pathways for retarding AS. This review summarizes the current knowledge of biomedical mechanisms by which rapamycin retards AS through action on various cells (endothelial cells, macrophages, vascular smooth muscle cells, and T-cells) in early and advanced AS and describes clinical and potential clinical applications of the agent.

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“…Discouraging the use of mTOR inhibition is the fact that rapamycin significantly attenuates both endothelial function and the expression of eNOS in human endothelial cell lines in vitro , although it does not cause endothelial cell death [ 144 ]. Studies with mTOR-inhibiting drugs, among others applied on coronary stents in patients with advanced arterial aging, have reported deleterious effects of such drugs on various variables of endothelial (dys)function, although conflicting results are abundant [ 145 , 146 , 147 , 148 , 149 ]. It is unclear whether the conflicting results are dependent on the concentration of the mTOR inhibitor to which the endothelial cells are exposed, which presumably is very high in the case of drug-eluting stents.…”

Section: Perspectivesmentioning

confidence: 99%

DNA Damage: A Main Determinant of Vascular Aging

Bautista-Niño

Portilla‐Fernandez

Vaughan

et al. 2016

IJMS

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Vascular aging plays a central role in health problems and mortality in older people. Apart from the impact of several classical cardiovascular risk factors on the vasculature, chronological aging remains the single most important determinant of cardiovascular problems. The causative mechanisms by which chronological aging mediates its impact, independently from classical risk factors, remain to be elucidated. In recent years evidence has accumulated that unrepaired DNA damage may play an important role. Observations in animal models and in humans indicate that under conditions during which DNA damage accumulates in an accelerated rate, functional decline of the vasculature takes place in a similar but more rapid or more exaggerated way than occurs in the absence of such conditions. Also epidemiological studies suggest a relationship between DNA maintenance and age-related cardiovascular disease. Accordingly, mouse models of defective DNA repair are means to study the mechanisms involved in biological aging of the vasculature. We here review the evidence of the role of DNA damage in vascular aging, and present mechanisms by which genomic instability interferes with regulation of the vascular tone. In addition, we present potential remedies against vascular aging induced by genomic instability. Central to this review is the role of diverse types of DNA damage (telomeric, non-telomeric and mitochondrial), of cellular changes (apoptosis, senescence, autophagy), mediators of senescence and cell growth (plasminogen activator inhibitor-1 (PAI-1), cyclin-dependent kinase inhibitors, senescence-associated secretory phenotype (SASP)/senescence-messaging secretome (SMS), insulin and insulin-like growth factor 1 (IGF-1) signaling), the adenosine monophosphate-activated protein kinase (AMPK)-mammalian target of rapamycin (mTOR)-nuclear factor kappa B (NFκB) axis, reactive oxygen species (ROS) vs. endothelial nitric oxide synthase (eNOS)-cyclic guanosine monophosphate (cGMP) signaling, phosphodiesterase (PDE) 1 and 5, transcription factor NF-E2-related factor-2 (Nrf2), and diet restriction.

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Head‐to‐head comparison of sirolimus‐eluting stent versus bare metal stent evaluation of the coronary endothelial dysfunction in the same patient presenting with multiple coronary artery lesions: The CREDENTIAL study

Abstract: in the same patients, but treating different coronary segments, SES implantation induces a higher rate of vasoconstriction compared to BMS. The increased vasoconstriction after iiAch is an indicator of ED.

Cited by 10 publications

References 18 publications

Prognostic Value of VEGF in Patients Submitted to Percutaneous Coronary Intervention

Prognostic Value of VEGF in Patients Submitted to Percutaneous Coronary Intervention

Rapamycin: A Bacteria-Derived Immunosuppressant That Has Anti-atherosclerotic Effects and Its Clinical Application

DNA Damage: A Main Determinant of Vascular Aging

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